Goodpasture’s Syndrome in a Patient Receiving Penicillamine and Carbimazole

Abstract

A 51-year-old woman with advanced rheumatoid arthritis developed a Goodpasture’s syndrome during treatment with penicillamine and carbimazole. Circulating antiglomerular basement membrane antibodies (anti-GBM) were present. Renal biopsy showed focal necrotizing glomerulonephritis with crescents, and HLA typing showed the presence of DR3 and DR4. The patient responded dramatically to pulse methylprednisolone and cyclophosphamide, with both clinical remission and disappearance of anti-GBM antibodies.

<i>D</i>-Penicillamine-lnduced Crescentic Glomerulonephritis and Antimyeloperoxidase Antibodies in a Patient with Scleroderma

“…Most commonly, ANA were present, but in some cases their presence could be attributed to the patients' underlying immunological condition. Anti-GBM antibodies were present in 1 patient [10], but renal deposition of anti-GBM antibodies was not seen in a kid ney biopsy performed 2 months after the start of therapy. p-ANCA were detected in 2 of 3 patients with rheumatoid arthritis in whom the test was performed [12.…”

“…8, 14], mesangial [8,15,17] and/or subendothelial [7,14,17] locations. In 3 other biopsies examined by EM, no deposits were seen; 1 of these biopsies was performed 2 months after treat ment was started [10], In all the patients reported in table 1, D-penicillamine was stopped. However, only those patients who also received immunosuppressive therapy had a good outcome.…”

“…and as late as 6 years after the start of therapy. In many cases, hemoptysis was also present leading some authors to refer to this illness as Goodpasture's syndrome [4,5,10,15,16,20], Clinically, renal involvement was severe with many patients requir ing dialysis. In all cases, serum complement was normal.…”

Antiglomerular Basement Membrane Antibody-Mediated Glomerulonephritis after Intranasal Cocaine Use

“…The stimulus for developing autoantibodies to this antigen is unclear, but there is speculation that they may be cross-reacting with a variety of infectious agents [16]. It has been observed after exposure to various inhalants that tobacco smoke is the most common injurious agent [17], although inhalation of hydrocarbon solvents [18], hard metal dust [19], D -penicillamine [20, 21], ischemia [22], and ultrasonic lithotripsy [12]have also been implicated. In addition, anti-GBM antibodies have been found in the sera of some p-ANCA-positive patients [22, 23].…”

Antiglomerular Basement Membrane Glomerulonephritis after Inhalation of Chemical Toxins

“…Factors able to induce the anti-GBM antibody re sponse are increasingly recognized: exposure to toxic compounds such as paraquat and hydrocarbon solvents, or to drugs such as penicillamine [5] should be looked for systematically. Recognition of inciting agents may have therapeutic as well as physiopathologie implications.…”